MCP-1: The Missing Link Between Obesity And Insulin Resistance
15 May 2006
Individuals diagnosed with metabolic syndrome often have excessive fatty tissue in and around their abdomen, high cholesterol, elevated blood pressure, and an inability to utilize insulin or blood sugar (insulin resistance) - symptoms that put them at high risk of coronary heart disease and stroke. The molecular mechanisms that link obesity and insulin resistance are the subject of intense investigation and are not completely understood.
In a study appearing online on May 11 in advance of print publication in the June issue of the Journal of Clinical Investigation, Yoshikazu Tamori and colleagues from Kobe University, Japan, show that the concentration of monocyte chemoattractant protein-1 (MCP-1) in fat cells and blood plasma was increased both in genetically obese diabetic mice as well as healthy mice in which obesity had been induced by feeding them a high-fat diet. Mice expressing an MCP-1 transgene in fat cells exhibited insulin resistance, increased infiltration of macrophages into fatty tissue, and high cholesterol levels.
In addition, these effects were not observed in mice lacking MCP-1 even when fed the high-fed diet. The results of this study suggest that MCP-1 links obesity and insulin resistance by the induction of an inflammatory response (macrophage infiltration) in fatty tissue. The authors suggest that blocking the interaction of MCP-1 and its receptor, known as CCR2, might provide the basis for development of new therapies for this syndrome.
TITLE: MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity
https://www.the-jci.org/article.php?id=26498
Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
http://www.jci.org/ Article 
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